ArticleGlycobiology2009
Modeling a congenital disorder of glycosylation type I in C. elegans: a genome-wide RNAi screen for N-glycosylation-dependent loci.
Article in Glycobiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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Who cites it
18 citing papers in PubMed, 25 citations in OpenAlex.
- Repurposing the HMG-CoA reductase inhibitor atorvastatin for SRD5A3-congenital disorder of glycosylation.Communications medicine · 2026Article
- Glycan remodelling of live adult Schistosoma mansoni worms by chemical inhibition of α-mannosidases.International journal for parasitology · 2026Article
- P-glycoprotein-9-mediated multidrug tolerance in Caenorhabditis elegans.Parasites & vectors · 2025Article
- Beyond Proteostasis: Lipid Metabolism as a New Player in ER Homeostasis.Metabolites · 2021Review
- A Great Catch for Investigating Inborn Errors of Metabolism-Insights Obtained from Zebrafish.Biomolecules · 2020Review
- Measurements of Physiological Stress Responses in C. Elegans.Journal of visualized experiments : JoVE · 2020Article
- MANF deletion abrogates early larval Caenorhabditis elegans stress response to tunicamycin and Pseudomonas aeruginosa.European journal of cell biology · 2019Article
- Article
- N-glycomic Complexity in Anatomical Simplicity:Frontiers in molecular biosciences · 2019Review
- N-glycoprotein macroheterogeneity: biological implications and proteomic characterization.Glycoconjugate journal · 2016Review
- RNAi screening of human glycogene orthologs in the nematode Caenorhabditis elegans and the construction of the C. elegans glycogene database.Glycobiology · 2015Article
- Activation of the endoplasmic reticulum unfolded protein response by lipid disequilibrium without disturbed proteostasis in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- A genome-wide RNAi screen in Caenorhabditis elegans identifies the nicotinic acetylcholine receptor subunit ACR-7 as an antipsychotic drug target.PLoS genetics · 2013Article
- Therapies and therapeutic approaches in Congenital Disorders of Glycosylation.Glycoconjugate journal · 2013Review
- The class I α1,2-mannosidases of Caenorhabditis elegans.Glycoconjugate journal · 2012Article
- A glycobiology review: carbohydrates, lectins and implications in cancer therapeutics.Acta histochemica · 2011Review
- Metabolic manipulation of glycosylation disorders in humans and animal models.Seminars in cell & developmental biology · 2010Review
- Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Inefficient glycosylation caused by defective synthesis of lipid-linked oligosaccharide donor results in multi-systemic syndromes known as congenital disorders of glycosylation type I (CDG-I). Strong loss of function mutations are embryonic lethal, patients with partial losses of function are occasionally born but are very ill, presenting with defects in virtually every tissue. CDG-I clinical expression varies considerably and ranges from very mild to severe, and the underlying cause of the variable clinical features is not yet understood. We postulate that accompanying defects in an individual's genetic background enhance the severity of CDG-I clinical phenotypes. Since so many protein structures and functions are compromised in CDG-I illnesses, the gene products that are dependent on N-linked glycosylation which cause lethality or particular symptoms are difficult to resolve. The power of genetic silencing that is a characteristic of C. elegans has allowed us to systematically dissect the complex glycosylation phenotype observed in CDG-I patients into specific glycan-dependent gene products. To accomplish this, we inhibited glycosylation with a sub-phenotypic dose of tunicamycin, reduced single genes by RNA interference, and then sought loci where the combination caused a synthetic or dramatically enhanced phenotype. This screen has identified genes in C. elegans that require N-linked glycans to function properly as well as candidate gene homologues that may enhance the clinical severity of CDG-I disorders in humans.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.